The present study was undertaken to determine the relative contributions of altered metabolic responses and excess food intake to the obesity and hyperinsulinemia of the ventromedial hypothalamic (VMH) syndrome. This experiment, employing an intragastric hyperalimentation protocol, was also designed to address the related issue of whether altered energy utilization serves as a compensatory strategy for reducing energy retention in the face of excess intake. Separate groups of VMH-lesioned and sham-lesioned female rats were fed, either orally or intragastrically, up to 200% of the calories ingested by a normally feeding intact rat. Both VMH-lesioned and intact rats became obese and hyperinsulinemic when hyperalimented for 30 days, but rats with lesions deposited 25% more fat than intact animals receiving an identical number of calories. Estimates of total carcass energy indicated that rats with lesions required 11% less calories than intact rats to retain identical levels of energy. Furthermore, intact hyperalimented rats failed to evidence the caloric wastage that has been reported to occur in orally fed rats that overeat cafeteria diets.